Chapter 40 Chronic Pain Management
Multidisciplinary chronic pain management
1. Why is multidisciplinary teamwork necessary for managing chronic pain? What are the components of such a multidisciplinary team? How are patients usually referred to a pain clinic?
2. How should the initial evaluation of a patient be carried out in the pain clinic? How is a treatment plan established for a patient evaluated in a chronic pain clinic?
3. Name some treatment modalities for the management of chronic pain.
4. List some of the psychological components of the chronic pain disease process. What is the potential value of the Minnesota Multiphasic Personality Inventory when evaluating patients with chronic pain?
Common pain syndromes
5. What is meant by the term low back pain? What is the usual pattern of recovery for patients presenting with low back pain?
6. How does the typical patient with low back pain present to a pain physician?
7. What are the pathophysiologic mechanisms which commonly contribute to low back pain?
8. How can chronic low back pain arising from the lumbar facet joints be distinguished from lumbar radiculopathy?
9. What are some warning signs on the initial history and physical when evaluating a patient with low back pain that may indicate significant physical comorbidity that should be promptly investigated?
10. How should a physician approach medical therapy for the most common presentations of low back pain?
11. What are the socioeconomic considerations of low back pain and its treatment? What are some risk factors for developing chronic low back pain?
12. What is neuropathic pain? What are some of the typical signs and symptoms of neuropathic pain?
13. What is postherpetic neuralgia?
14. What treatment modalities have been used for the treatment of postherpetic neuralgia?
15. What are some of the side effects of tricyclic antidepressants that may limit their usefulness in elderly patients with postherpetic neuralgia?
16. What is diabetic peripheral neuropathy? How does it present?
17. What is complex regional pain syndrome? What differentiates type I and type II complex regional pain syndromes?
18. What are the clinical manifestations of complex regional pain syndrome?
19. How is the diagnosis of complex regional pain syndrome of the upper or lower extremity made?
20. What is the treatment for complex regional pain syndrome? How does the time delay to diagnosis and treatment affect treatment outcome?
21. What pharmacologic agents are commonly used for intravenous regional sympathetic nerve blockade? How is this technique believed to work?
Cancer-related pain
22. What are the various ways in which cancer can cause pain? What is the primary treatment for cancer pain?
23. What are some oral analgesics used to treat persistent cancer pain? What is the World Health Organization stepwise approach to managing cancer-related pain?
24. When oral intake by patients is limited, what are some alternative routes of analgesic drug delivery used to manage persistent cancer pain?
25. What are some neurosurgical procedures for the treatment of chronic pain that may be useful in cancer patients in whom less invasive procedures have been unsuccessful in providing pain control?
26. Which is the most common uniformly efficacious neurolytic block for visceral malignancy? What are the limitations of such a block?
Pharmacologic management of chronic pain
27. What are some of the pharmacologic agents used for pain management?
28. What are simple analgesics and how can they be useful in chronic pain management? How are cyclooxygenase-2 selective drugs useful for chronic pain management and how do they differ from nonselective drugs?
29. How do antidepressants exert their actions? List some antidepressants commonly used for pain management and their side effects.
30. Which anticonvulsants are commonly used for pain management? What are the most common side effects associated with each agent? What are the first-line treatments for neuropathic pain?
31. What potential problems are encountered by physicians when prescribing opioids?
32. What basic principles guide the use of opioids in terminally ill patients as compared with those with nonmalignant chronic pain?
33. What are the current guidelines for the stepwise pharmacologic management of neuropathic pain?
Interventional pain therapies
34. What is meant by the term interventional pain therapy? Name some of the commonly performed interventional procedures used to treat pain.
35. How is an epidural steroid injection useful as an interventional therapeutic procedure? What side effects should patients be informed about?
36. What are the different techniques used to inject steroids into the epidural space? What is the rationale for using one technique over another?
37. When should a physician suspect the facet joint as a cause of low back pain? How can a facet joint block be useful as a diagnostic tool?
38. What is the role of radiofrequency ablation in the long-term management of persistent facet-related pain?
39. What is the current role of lumbar diskography in the management of lumbosacral pain?
40. What is minimally invasive disk decompression? How does it work and what is a limitation of this procedure?
41. How are sympathetic nerve blocks useful as a diagnostic tool in chronic pain management? What is the current evidence of their role in managing chronic pain syndromes?
42. What is the anatomical location of stellate ganglion? How is a stellate ganglion block useful in the management of chronic pain?
43. How is a stellate ganglion block performed? Describe a safer alternative to the conventionally performed stellate ganglion block.
44. List the common conditions for which stellate ganglion block is used in treatment.
45. What are the signs of a successful stellate ganglion block?
46. What are the complications of stellate ganglion block?
47. What is the anatomic location of the celiac plexus and what are the structures that lie immediately adjacent to the celiac plexus?
48. What are the most common techniques by which a celiac plexus block can be performed?
49. What is the clinical indication for a celiac plexus block?
50. How does a celiac plexus block differ from a splanchnic nerve block?
51. What are the complications associated with celiac plexus block?
52. Describe the applied anatomy of the lumbar sympathetic chain.
53. What are some of the clinical uses of a lumbar sympathetic block? List the complications that may be encountered while performing a lumbar sympathetic block.
54. What fundamental physiologic principle forms the basis of spinal cord stimulation?
55. What is the current role of spinal cord stimulation in managing chronic pain syndromes?
Answers*
Multidisciplinary chronic pain management
1. Chronic pain is a complex disorder and patients suffering from chronic pain usually have biologic disease that coexists with cognitive, affective, behavioral, and social factors. Hence, management of such a disease process requires the expertise of health care providers from a range of medical specialties. The team at most centers consists of a physician, often an anesthesiologist, a psychologist, and a physical therapist working together. Patients are usually referred to a chronic pain clinic by their primary care physicians for a problem with chronic pain that has not responded to conventional medical therapy.
2. On his or her arrival to a chronic pain clinic, the patient should be evaluated by a physician with expertise in pain medicine. During the initial evaluation, the potential psychological, medical, and social contributions to the patient’s pain should be evaluated. While it would be ideal for a psychologist and a physical therapist to also evaluate each new patient and then this multidisciplinary team meet to discuss the various aspects of the patient’s history, as well as a probable diagnosis, this is seldom possible in today’s constrained health care environment. Nonetheless, the physician who conducts the initial evaluation must devise a treatment plan for each patient that takes into consideration all aspects of the patient’s care and arranges for appropriate referral to other members of the team when needed. (699)
3. Treatment modalities available in most chronic pain clinics include oral pharmacotherapy, diagnostic and therapeutic nerve blocks, the neuraxial administration of opioids, neurostimulation techniques, biofeedback, and physical therapy. (699)
4. Chronic pain as a disease process may include psychiatric and psychological manifestations, some of which include depression, insomnia, and avoidance of social and vocational obligations. Dependence on analgesics and visits to multiple physicians are common among patients with chronic pain. The Minnesota Multiphasic Personality Inventory is a useful test for the detection of many of these common comorbidities that often coexist in those suffering with chronic pain. (699)
Common pain syndromes
5. Low back pain (LBP) is the most common reason why people seek medical attention and is also known as lumbosacral pain. This refers to pain in either the lumbar or the sacral spinal region. Anatomically, the region is defined as the area of the back between the tip of the twelfth thoracic spinal process up till the sacrococcygeal joint. Most people presenting with low back pain recover with no treatment. A majority recover by 6 weeks (60% to 70%) or mostly by 12 weeks (90%). The recovery after 12 weeks, however, is slow and uncertain. (699, Figure 43-1)
6. Patients presenting with low back pain usually have pain either localized to the back region (acute or chronic lumbosacral pain) or distributed in the area of nerve (acute or chronic radicular pain). Acute radicular pain is typically caused by a herniated nucleus pulposus in younger patients. Signs of radiculopathy include numbness, weakness, or loss of deep tendon reflexes in the area of the affected nerve. In the elderly, foraminal narrowing may affect the spinal nerve leading to acute radicular pain. Patients presenting with chronic radicular pain require a detailed search for a reversible cause of nerve root impingement. MRI or electrodiagnostic testing could give some clues to the cause of pain in patients who have had prior surgery. Acute lumbosacral pain with no radicular symptoms in most cases may be myofascial in origin and require no further radiologic investigation. Chronic lumbosacral pain may arise from many parts of the vertebral unit; most commonly implicated are the sacroiliac joint, lumbar facets, and the intervertebral disks. Diagnostic nerve blocks involving injection of local anesthetic at these anatomic sites leading to temporary pain relief can aid in localizing the origin of pain. Diagnosis and treatment of the patient with low back pain rely on the location of pain (primarily radicular or lumbosacral) and the duration of symptoms (acute or chronic). (700-701)
7. The following pathophysiologic mechanisms result from degenerative changes in the spinal functional unit due to aging and injury, and can give rise to lumbosacral and/or lumbar radicular pain:
Synovitis in the facet joints leading to capsular laxity and subluxation; facet-related pain is predominantly localized over the lumbosacral junction.
8. Pain arising from the lumbar facet joint is predominantly localized near the lumbosacral junction, while lumbar radicular pain is localized within the leg. The pain arising from facet joints is usually diagnosed by the injection of a small volume of local anesthetic into the joint under fluoroscopic guidance. Substantial pain relief suggests that pain originates from inflammation of that particular joint. However, a substantial number of patients will report pain reduction even when a nonactive agent such as normal saline is injected. This placebo response can complicate certain diagnosis using diagnostic injections. (700)
9. When first evaluating a patient with back pain, the physician should be aware of certain conditions that may indicate significant physical comorbidity, prompting further investigation. In the patient’s history, these include new onset or worsening pain after trauma, infection, or previous malignancy. Patients who report worsening neurologic deficits, or bladder or bowel dysfunction, warrant early radiologic imaging to rule out neural compression. (700)
10. Medical therapy for the most common presentations of low back pain is based on how a patient presents to the pain physician and on the duration of pain symptoms. Acute radicular pain: Therapy is usually started with a 7-day course of simple analgesics alone or in combination with an opioid analgesic and a muscle relaxant for associated muscle spasm. Chronic radicular pain: Therapy usually begins with a trial of antidepressants or anticonvulsants since opioids are less effective for neuropathic pain. Patients who are poor responders to combination medical therapy are offered a trial of spinal cord stimulation. Acute lumbosacral pain is usually managed with a short course of a simple analgesic alone or in combination with an opioid and a muscle relaxant as needed. Pharmacotherapy is usually followed by physical therapy for patients with persistent pain. First-line management for patients with chronic lumbosacral pain involves diagnostic medial branch nerve blocks to rule out facet joint pain. If positive, radiofrequency treatment may prove beneficial. For patients with continued pain, a formal physical and behavioral therapy program is usually recommended. (705, Table 43-4)
11. Low back pain and its treatment place a huge socioeconomic burden on society. Only 40% to 45% of the patients who are disabled for 6 months will ever return to work. The return to work rate for patients absent for 2 years is close to zero. The risk factors for developing chronic low back pain include age, gender, socioeconomic status, body mass index, tobacco use, general health status, strenuous physical activities, job dissatisfaction, depression, and anatomic variations. (699)
12. Neuropathic pain is persistent following injury to the nervous system. The three most common types of neuropathic pain include postherpetic neuralgia, diabetic peripheral neuropathy, and complex regional pain syndrome. Patients with neuropathic pain often report:
13. Postherpetic neuralgia refers to pain that persists for extended periods of time (more than 3 to 6 months) after an acute infection of herpes zoster. Postherpetic neuralgia usually occurs in elderly or immune compromised patients due to a secondary infection of varicella zoster virus (called shingles) leading to damage to small unmyelinated nerve fibers. The pain is characterized by episodic lancinating pain accompanied by severe allodynia in the affected dermatome. In recent years the availability of a vaccine has reduced the incidence of postherpetic neuralgia. (702)
14. Postherpetic neuralgia has been treated with occasional success with sympathetic nerve blocks in patients who have sought early treatment, but sympathetic blocks are ineffective in those with established postherpetic neuralgia. Treatment of established postherpetic neuralgia is challenging. Tricyclic antidepressants and anticonvulsants remain the mainstay of treatment. Topical lidocaine is useful to reduce the painful allodynia. (702)
15. Side effects of tricyclic antidepressants include orthostatic hypotension, sedation, urinary retention, and an increase in appetite. Tricyclic antidepressants may also cause worsening of preexisting heart block. These side effects may limit the usefulness of tricyclic antidepressant medication therapy in elderly patients suffering from postherpetic neuralgia. (704)
16. Diabetic peripheral neuropathy, the most common cause of neuropathic pain, occurs as a result of damage to small unmyelinated nerve fibers. The symptoms are numbness associated with paresthesias, dysesthesias, and pain commonly described as burning or deeply aching. Symptoms can progress slowly over many years, and may affect the hands as well as the lower extremities. Diabetic patients with poor glucose control are at the greatest risk for developing diabetic peripheral neuropathy. (702)
17. Complex regional pain syndrome (CRPS) refers to signs and symptoms that emerge in certain patients after injury to peripheral nerves, typically after trauma to an extremity. After the initial trauma, and during healing, persistent neuropathic pain associated with sympathetic nerve dysfunction develops and is characterized by swelling, edema, erythema and temperature changes. The term CRPS type I, also called reflex sympathetic dystrophy, is used when pain occurs without an identifiable injury to a major nerve (e.g., ankle sprain). CRPS, type II, also called causalgia, presents with the same signs and symptoms but following an identifiable nerve injury (e.g., a pelvic fracture with a partial sciatic nerve transection). (702-703)
18. Clinical manifestations of complex regional pain syndrome include chronic, severe burning pain, hyperalgesia, bone demineralization, joint stiffness, and atrophic changes. Patients typically have localized sympathetic nervous system dysfunction, which is manifest as warm, erythematous, dry, and swollen skin early in the disease process, followed by vasoconstriction, with cool, pale, and edematous skin later in the course. Patients usually characterize the pain in these syndromes as aching, intense, and/or agonizing. The pain appears to be enhanced by mechanical stimulation, movement, and the application of heat or cold. (702, Table 43-1)
19. The diagnosis of complex regional pain syndrome is based on the appearance of the typical signs and symptoms after injury and the absence of any other underlying condition. Some practitioners have suggested that the diagnosis can be made by performing sympathetic nerve blocks in the affected extremity and evaluating the patient for relief of the pain. For the upper extremity a stellate ganglion block may be performed, while for the lower extremities lumbar sympathetic blocks are usually performed. However, there is a significant placebo response to diagnostic blocks, and the true role of sympathetic blocks in the diagnosis and management of CRPS remains in question. (703)
20. The management of CRPS requires a multimodal approach. The primary goal of managing patients diagnosed with CRPS is maintenance and restoration of function through aggressive physical therapy, which is possible only with adequate pain reduction. Sympathetic nerve blocks often aid in short-term pain reduction and hence facilitation of physical therapy. Tricyclic antidepressants and anticonvulsants usually form the first line of analgesic therapy. Spinal cord stimulation is now used more commonly and may provide a more effective long-term means to produce pain reduction, hence facilitating long-term physical therapy aimed toward functional restoration of the affected extremity. A delay in the diagnosis and treatment of complex regional pain syndrome may result in poorer outcome. (703)
21. Intravenous regional sympathetic nerve blockade has been used for the treatment of complex regional pain syndromes. Pharmacologic agents that have been used for intravenous regional sympathetic nerve blockade include guanethidine and bretylium. Guanethidine is taken up by presynaptic sympathetic nerve terminals where it is concentrated in norepinephrine neurotransmitter vesicles and replaces norepinephrine, thereby blocking norepinephrine release. Bretylium blocks norepinephrine release from nerve terminals. These agents are believed to exert their analgesic effects in sympathetically maintained states by blocking norepinephrine release from sympathetic nerve terminals. Neither agent is now commonly used: guanethidine is not available for clinical use in the United States and bretylium is associated with profound hypotension. More commonly, intravenous regional blocks are conducted with local anesthetic alone, typically 0.5% lidocaine; careful attention must be paid to avoid toxic levels of local anesthetic. The relative effectiveness of intravenous regional blockade versus sympathetic ganglion blocks is unknown. (703)
Cancer-related pain
22. Pain is the most common presenting symptom of undiagnosed malignancy. Cancer pain may be due to direct invasion of the malignancy or treatment. Local tumor infiltration or metastases to bone or nerves are especially painful. Patients may also experience pain as a side effect of chemotherapy, irradiation, or surgical treatment. Examples include phantom limb pain, peripheral neuropathy, and radiation fibrosis. Approximately 40% of patients with cancer experience chronic pain. The primary focus of pain reduction in patients with cancer is direct treatment of the malignancy, with successful treatment often leading to complete pain resolution. (703)
23. The mainstay of treatment of chronic pain for cancer patients is opioid therapy. Other analgesics which are commonly used are tricyclic antidepressants, anticonvulsants, and corticosteroids. Tricyclic antidepressants may have additional benefits of treating depression (common among cancer patients), potentiating the effect of opioids, facilitating nocturnal sleep, and improving mood. Anticonvulsant medications may be useful in neuropathic pain. Corticosteroids play a role in decreasing the sensation of pain, improving mood, and increasing appetite, all of which are ongoing problems in patients with chronic cancer pain. The World Health Organization’s analgesic approach has been adopted worldwide to promote the aggressive treatment of cancer-related pain by tailoring analgesic use to the severity of pain. It comprises a simple three-step analgesic ladder starting with nonopioids and moving toward more potent opioid analgesics as necessary to control pain. (703, Table 43-2)
24. Intravenous, neuraxial, transdermal, and transmucosal routes of administration are alternative routes of analgesic drug delivery for the cancer patient with chronic pain in whom the oral administration of medicines is not possible. Implantable intrathecal drug delivery systems using intrathecal opioids, local anesthetics, clonidine, and other agents are now often used in managing intractable cancer pain. (703)
25. Patients with chronic pain secondary to cancer who have not had success with pain control with less invasive procedures may benefit from some neurosurgical procedures for the treatment of the pain. Neurosurgical procedures that may be useful in these cancer patients include a cordotomy or dorsal rhizotomy. A cordotomy is the open or percutaneous interruption of the spinothalamic tract. A dorsal rhizotomy is the interruption of the sensory nerve root.
26. One of the most common nerve blocks that successfully treats abdominal visceral malignancy is the neurolytic celiac plexus block. The neurolytic celiac plexus block (NCPB) may be useful to treat pain associated with cancer of the pancreas or upper abdominal viscera. One limitation of this block is the inability to treat pain from the left colon and pelvic viscera as the sensory and autonomic nervous system fibers only from the abdominal viscera are carried by the celiac plexus. NCPB has a long-lasting benefit for 70% to 90% of patients with abdominal visceral malignancies. (710)
Pharmacologic management of chronic pain
27. Pharmacologic agents used for pain management include nonsteroidal antiinflammatory agents, antidepressants, anticonvulsants, muscle relaxants, and opioids. Opioid analgesics are the most common agents used in the management of cancer-related pain, but their long-term benefit in managing patients with noncancer pain remains unclear. The antidepressants and anticonvulsants are the most common agents used for the long-term treatment of chronic neuropathic pain. Nonsteroidal antiinflammatory drugs and muscle relaxants are useful in the management of acute pain, but the risk/benefit ratio of long-term use is less clear. (704, Table 43-3)
28. The term simple analgesic has been traditionally reserved for acetaminophen and the nonsteroidal antiinflammatory drugs (NSAIDs). They are the most common agents used to treat mild to moderate pain. Even though poorly supported by evidence for use in chronic illnesses such as low back pain, the use of NSAIDS remains fairly common. They may be useful in conjunction with opioids for the treatment of chronic pain in patients with pain that involves an inflammatory process or in patients with bone pain such as arthritis. They also constitute the first step of the WHO analgesic ladder and are used to treat mild to moderate cancer-related pain. Enzyme selective NSAIDs (i.e., the COX-2-selective inhibitors) have a lower risk of GI bleeding as compared to nonenzyme selective drugs, even though they are comparable in their analgesic efficacy. (703)
29. Antidepressants are thought to exert their effect by normalizing sleep patterns, decreasing anxiety, and decreasing the patient’s perception of the pain. Antidepressants may enhance neurotransmitters acting on descending efferent inhibitory pain pathways, thus producing analgesia that is independent of their antidepressant effects. Antidepressants commonly used for the management of chronic pain include tricyclic antidepressants and newer selective norepinephrine reuptake inhibitors (SNRIs). Examples of tricyclic antidepressants include the secondary amine agents (nortriptyline and desimipramine) and tertiary amine agents (amitriptyline and imipramine), which are more poorly tolerated. Side effects of tricyclic antidepressants include dry mouth and urinary retention, and potentially worsening of preexisting heart block. The newer SNRIs (venlafaxine, duloxetine) are effective in treatment of neuropathic pain, such as painful diabetic peripheral neuropathy. Though SNRIs have a similar analgesic efficacy as tricyclic antidepressants, they are better tolerated because of a favorable side effect profile. (704)
30. The anticonvulsant drugs gabapentin and pregabalin are effective for pain management. These drugs are commonly used as they are fairly well tolerated with mild to moderate side effects like somnolence, drowsiness, and peripheral edema. They are also commonly used to treat all types of neuropathic pain. The choice of neuropathic agent should be guided by the severity of the pain and the side effect tolerability by each patient. (704)
31. Use of long-term opioid therapy for the treatment of chronic noncancer pain remains controversial. The most common problems encountered by physicians when prescribing opioids are aberrant drug-related behavior (e.g., losing prescriptions, unauthorized escalation of drug dose) and opioid tolerance (need for increasing drug dose to produce the same effect). Overt addiction (i.e., preoccupation with use of the opioid despite negative consequences like job loss) is uncommon. (704)
32. Opioid analgesic prescribing for nonmalignant chronic pain is adapted from cancer pain management. This practice involves using a long-acting opioid for continuous analgesia while a short-acting analgesic is used to cover intermittent spikes in pain intensity, or breakthrough pain. However, the long-term use of opioids has come under increasing scrutiny for managing noncancer pain, thus adopting more stringent guidelines is wise. Most practitioners agree that opioids should be used only when other, more conservative measures have failed. Patients should receive these medications from a single prescriber and they should only be continued when they lead to less pain and improvement in function. Many practitioners have adopted routine use of random urine drug testing to help ensure that patients remain compliant with chronic opioid therapy and that they are not using other prescription or illicit drugs. (704)
33. Evidence-based guidelines for the pharmacologic management of neuropathic pain recommend a stepwise pharmacologic approach. Following initial assessment and diagnosis, realistic goals should be discussed with the patient. Therapy is usually begun with a tricyclic antidepressant, SNRI, or anticonvulsant as the first-line drug, followed by opioids or tramadol, alone or in combination (second-line drugs). Serial follow-ups are conducted to evaluate response to therapy and alternative first- or second-line drugs are commenced based on the response. Certain antiepileptics, antidepressants, and NMDA receptor antagonists can be used as a third line of drugs for a selective group of patients who respond poorly to the previous therapy. (704, Table 43-3)
Interventional pain therapies
34. The term interventional pain therapy encompasses a variety of treatments used for specific pain syndromes and these range from diagnostic nerve blocks to therapeutic injections of steroids and sympathetic nerve blocks. Some of the commonly performed procedures in the pain clinic include: epidural steroid injections, facet joint nerve blocks, and radiofrequency ablation. (705)
35. The injection of steroid into the epidural space is aimed at the inflammatory response that is associated with acute disk herniation. Epidural steroids are most useful for treating acute radicular pain, where a steroid injection if given within 6 weeks can accelerate the resolution of leg pain. Patients should be informed about pain at the injection site and transient worsening of any radicular pain if present on presentation. Infection, bleeding, and neural injury are all uncommon and discussions about these rare complications should be based on individual patient concerns. (705-706)
36. Epidural injection of steroids can be done using either the interlaminar or transforaminal approach. The transforaminal approach may be more effective as it allows the concentrated steroid solution to be injected directly adjacent to the spinal nerve close to the site of the inflammation, yet there is little scientific evidence to guide the choice between these two approaches. (706, Figures 43-4, 43-5)
37. One of the many causes of low back pain is pain arising from the facet joints. Facet-related pain should be suspected in patients who have persistent pain over in the lumbosacral area, and have typical patterns of referred pain with maximal tenderness directly over the facet joints. Facet joint blocks are commonly used as a diagnostic tool and involve intraarticular injections of a mixture of local anesthetic and corticosteroids. Intermediate pain relief lasting weeks to months is common and supports the diagnosis of facet-related pain. (706)
38. Radiofrequency denervation of the lumbar facet joints can provide longer duration of pain relief than intraarticular injections in some patients with facet-related pain. About 50% of patients will respond with a 50% reduction of pain lasting for up to 12 months. Radiofrequency denervation involves the delivery of energy adjacent to the sensory nerve in the facet joint. The procedure can be repeated with similar efficacy after repeat treatment. (706, Figure 43-6)
39. The use of lumbar diskography is based on the hypothesis that the intervertebral disk is the source of ongoing pain in about 30% to 40% of the patients presenting with lumbosacral pain. Provocative diskography is currently used to select patients for surgical fusion but has largely remained a controversial test because of the subjective nature of the test and the lack of convincing evidence that use of diskography improves surgical outcome. Diskography has also been used to select patients for intradiscal electrothermal therapy (IDET), a treatment that uses thermal energy to treat discogenic pain. Evidence for use of IDET is mixed; in some reports, 30% to 50% of patients showed long-term pain reduction and improvement in standing and sitting tolerance. The use of both diagnostic diskography and IDET has declined in recent years. (706)
40. Percutaneous plasma disk decompression (PDD) is a minimally invasive procedure used to treat chronic radicular pain due to a focal disk bulge identified on imaging studies, usually MRI. PDD reduces pain and improves long-term functional status in highly selected patients—those with ongoing leg pain and small disk protrusions. The procedure uses radiofrequency energy to remove a portion of nucleus pulposus, which eases the pressure of the disk and hence decompresses any pressure on the spinal nerve causing pain. A major limitation of this technique is that it is only useful for patients with herniations smaller than 3 mm, and this comprises less than 5% of patients with low back pain. (707)
41. Certain pain syndromes such as CRPS and microvascular insufficiency causing ischemic extremity pain are believed to be maintained by hyperactivity of the sympathetic nervous system and are termed sympathetically maintained pain syndromes. Blockade of the sympathetic nerve fibers produces pain relief in these disease states and these nerve blocks are hence often used to diagnose CRPS and related syndromes. There is a paucity of evidence supporting the use of repeated sympathetic blocks to provide long-term pain relief or improvement in function; however, these nerve blocks are still used to provide short-term pain relief and facilitate physical therapy. (707-708)
42. The stellate ganglion is formed by the fusion of the inferior cervical and the first thoracic sympathetic ganglia. There is significant anatomic variation in the cervical and thoracic sympathetic chain and in many individuals the superior thoracic and inferior cervical ganglia are separate structures. On the medial side of the ganglion is the lateral border of the longus colli muscle. Posteriorly are the neck of the first rib and the transverse process of the seventh cervical vertebra. Anteriorly lay the first part of the subclavian artery and the origin of the vertebral artery behind the dome of the lung. Anatomically, the sympathetic supply of the head, neck, and the arms passes through the stellate ganglion on each side. Hence a stellate ganglion block is performed to diagnose and treat sympathetically maintained pain of the head, neck, and the upper extremity. (708, Figure 43-7)
43. The most common approach to the stellate ganglion is the anterior paratracheal approach guided by surface anatomy of the C6 vertebra. When performing the block without radiographic assistance, the operator palpates the anterior tubercle of the transverse process of the C6 vertebra then retracts the overlying carotid artery and jugular vein laterally. A needle is advanced until seated on the anterior tubercle of C6, where about 10 mL of local anesthetic is injected incrementally. The local anesthetic spreads along the prevertebral fascia in the caudal direction to bathe the stellate ganglion. Another approach that has been used is approaching the ganglion at the level of C7; however, this carries a substantial risk of pneumothorax because the dome of the lung lies in close approximation to the needle injection site. When performed under radiographic assistance, the needle is placed just inferior to the uncinate process of the C6 or C7 vertebra near the junction of the transverse process and the vertebral body. (708)
44. A stellate ganglion block is used to diagnose and treat painful syndromes involving the upper extremity, most commonly CRPS. There is some evidence that it may also be useful for treating neuropathic pain arising from ischemia, herpes zoster, early postoperative neuralgia, and postradiation neuritis. Stellate ganglion block has also been used in the treatment of some disease states associated with vascular compromise, including intractable angina pectoris, Raynaud disease, frostbite, vasospasm, and occlusive or embolic phenomena. Stellate ganglion block has shown usefulness in controlling hyperhidrosis of the upper extremity. (709)
45. Successful stellate ganglion block is signaled by the appearance of Horner syndrome, a constellation of signs and symptoms which includes miosis (pupillary constriction), ptosis (drooping of the upper eyelid), and enophthalmos (sunken eyeball). Other signs of a successful block include nasal congestion, anhidrosis (lack of sweating), and venodilation in the involved extremity. There will also be an increase in local temperature by at least a degree Celsius in the affected extremity. Thus there are several signs the clinician should look for to confirm success of a stellate ganglion block. (708)
46. Stellate ganglion block is associated with the following minor and major complications. Minor complications include a recurrent laryngeal nerve block causing hoarseness, phrenic nerve blockade leading to unilateral diaphragmatic paresis, and somatic blockade of the upper extremity (brachial plexus block) characterized by sensory and motor loss on the ipsilateral side. Major complications include intravascular injection of local anesthetic causing immediate seizures, and epidural or intrathecal injection of the local injection causing a neuraxial block. The complication of a neuraxial block can be a high epidural or spinal with loss of consciousness and apnea, for which immediate resuscitation would be required. (709)
47. The celiac plexus is comprised of a diffuse network of nerve fibers that lie over the anterior surface of the aorta at the T12-L1 vertebral level surrounding the origin of the celiac artery from the aorta. Presynaptic nerve fibers travel from the sympathetic chain toward the ganglion over the anterolateral aspect of the inferior thoracic vertebra as the greater, lesser, and least splanchnic nerves. Postsynaptic fibers innervate all the abdominal viscera, including the gastrointestinal tract between the gastroesophageal junction and the splenic flexure of the colon. Sympathetic fibers to the descending and sigmoid colon, the rectum, and the pelvis do not travel through the celiac plexus. (710, Figure 43-8)
48. A neurolytic celiac plexus block (NCPB) can be performed using either a transcrural or a retrocrural approach. The transcrural technique consists of placing the neurolytic agent directly on the celiac ganglion anterolateral to the aorta. This approach reduces the chance of nerve root involvement. The retrocrural approach involves positioning the needles posterior to the diaphragmatic crura in close apposition to the T12 vertebral body. The percutaneous posterior approach is performed using surface anatomic landmarks to position needles in the vicinity of the celiac plexus. NCPB is then achieved with the injection of 20 to 30 mL of either alcohol (50% to 100%) or phenol (10% to 12%). The position of the needle can be verified by computed tomography (CT), fluoroscopy, or ultrasound (using an endoscopic ultrasound-guided transgastric approach). No single technique has proven superior to the other. (710)
49. A neurolytic celiac plexus block is used to control pain arising from intraabdominal structures, including the pancreas, liver, gallbladder, omentum, mesentery, and the gastrointestinal tract from the stomach to the transverse colon. Most often the source of the pain is malignancy, particularly pancreatic cancer. The pain relief for these patients can be dramatic, and has long-lasting benefit for 70% to 90% of patients. The use of the NCPB for nonmalignant pain, such as those with chronic pancreatitis, is debatable. (711)
50. During NCPB, a transcrural approach places the neurolytic agent directly on the celiac ganglion, anterolateral to the aorta, while a retrocrural approach places the solution posterior to the diaphragmatic crura in close apposition to the T12 vertebral body. A splanchnic nerve block is a minor modification to the classic retrocrural celiac plexus block; the only difference being that for a splanchnic nerve block, the needles are placed in the midportion of T12 rather than in the cephalad portion of L1 as is done for a celiac plexus block. (710)
51. The normal and expected physiologic effects of producing a sympathetic block to the abdominal viscera are diarrhea from unopposed parasympathetic stimulation of the bowel and orthostatic hypotension from splanchnic vasodilation. There are other potential complications of a neurolytic celiac plexus block. Intravascular injection of 30 mL of 100% ethanol results in a blood ethanol level high enough to produce intoxication. Intravascular injection of 30 mL of 10% phenol will cause clinical manifestations similar to local anesthetic toxicity, including seizures, cardiac arrhythmias, and even cardiovascular collapse. Perhaps the most feared complication of NCPB is paraplegia. Segmental spread at the level of T12 or L1 may cause spasm or even necrosis of the artery of Adamkiewicz, which compromises the blood supply of the anterior two thirds of the spinal cord in the low thoracic region. Best available estimates of the incidence of paraplegia place the risk at less than 1:1000. (711)
52. The lumbar sympathetic chain consists of four to five paired ganglia that lie over the anterolateral surfaces of the L2-L4 vertebra. Their cell bodies lie in the anterolateral region of the spinal cord from T11 to L2, where the preganglionic fibers exit the spinal canal with the corresponding spinal root, join the sympathetic chain, and then synapse with the appropriate ganglion. Postganglionic fibers exit the ganglion to form a diffuse network of perivascular fibers surrounding the vessels in the lower extremities; postganglionic fibers also travel within the nerves of the lumbosacral plexus. (711, Figure 43-9)
53. Lumbar plexus block is used in the diagnosis and treatment of sympathetically maintained pain of the lower extremities (e.g., CRPS types I and II). It is also used clinically to treat ischemic pain from small vessel occlusion in the lower extremities. There is some evidence supporting the usefulness of lumbar sympathetic block for treating painful neuropathic states of the lower extremities, including early postherpetic neuralgia and acute herpes zoster. Complications are uncommon with proper use of a lumbar sympathetic block. Toxic levels of local anesthetic can result from an inadvertent intravascular injection while performing a lumbar sympathetic block, and if large volumes of concentrated local anesthetic are used, the local anesthetic toxicity could be catastrophic. Some other complications which could be encountered include hematuria caused by direct needle placement through the adjacent kidney, spinal nerve injury, and epidural or intrathecal injection of local anesthetic. All are uncommon complications when the procedure is performed under radiographic guidance. Following neurolysis of the lumbar sympathetic chain, postsympathectomy pain in the distribution of the L1 spinal nerve (anterior thigh) occurs in about 10% of patients. (712)
54. Spinal cord stimulation is based on the hypothesis that a nonnoxious stimulus interferes with the perception of pain. This input of a nonpainful stimulus directly activates the ascending fibers within the dorsal columns of the spinal cord that transmit nonpainful stimuli and this principle is used to treat chronic back pain. A typical spinal cord stimulator system is comprised of a pacemaker-like implanted pulse generator connected to an electrode positioned over the dorsal columns of the spinal cord in the posterior epidural space. (712)
55. Current evidence supports the use of spinal cord stimulation (SCS) to treat pain, in particular for patients presenting with chronic lumbosacral pain or radicular pain after prior lumbar surgery. The evidence for the use of SCS for lumbosacral pain has been inconclusive, but with the advent of new dual lead systems and electrode arrays providing a broader area of stimulation, SCS may become more useful for treating pain in these patients. Management of chronic radicular pain using SCS is the best studied indication with the highest overall rate of successful long-term pain reduction. SCS has proven to be less expensive and more successful than repeat surgery in the management of persistent pain after prior lumbar surgery. (712)
56. The most common complication associated with SCS is lead displacement with the need for reoperation to reposition the lead(s). In modern case series, less than 5% of patients experienced wound infection or dehiscence. (712)
